The Anti-Inflammatory Effects and Mechanisms of Eupafolin in Lipopolysaccharide-Induced Inflammatory Responses in RAW264.7 Macrophages

被引:54
作者
Chen, Chin-Chaun [1 ,2 ,3 ]
Lin, Ming-Wei [6 ]
Liang, Chan-Jung [4 ,5 ]
Wang, Shu-Huei [6 ]
机构
[1] Chang Gung Univ, Grad Inst Nat Prod, Taoyuan, Taiwan
[2] Chang Gung Univ, Hlth Aging Res Ctr, Chinese Herbal Med Res Team, Taoyuan, Taiwan
[3] Chang Gung Mem Hosp, Tissue Bank, Taoyuan, Taiwan
[4] Kaohsiung Med Univ, CLGR, Kaohsiung, Taiwan
[5] Kaohsiung Med Univ Hosp, CLB, Kaohsiung, Taiwan
[6] Natl Taiwan Univ, Dept Anat & Cell Biol, Coll Med, Taipei, Taiwan
关键词
NF-KAPPA-B; LUNG EPITHELIAL-CELLS; RAW; 264.7; MACROPHAGES; NITRIC-OXIDE; SIGNALING PATHWAYS; GENE-EXPRESSION; ACTIVATION; MAPK; L; NEUROTOXICITY;
D O I
10.1371/journal.pone.0158662
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Eupafolin is a flavone isolated from Artemisia princeps Pampanini (family Asteraceae). The aim of this study was to examine the anti-inflammatory effects of eupafolin in lipopolysaccharide (LPS)-treated RAW264.7 macrophages and LPS-induced mouse skin and lung inflammation models and to identify the mechanism underlying these effects. Eupafolin decreased the LPS-induced release of inflammatory mediators (iNOS, COX-2 and NO) and proinflammatory cytokines (IL-6 and TNF-alpha) from the RAW264.7 macrophages. Eupafolin inhibited the LPS-induced phosphorylation of p38 MAPK, ERK1/2, JNK, AKT and p65 and the nuclear translocation of p65 and c-fos. These effects were mainly mediated by the inhibition of JNK. In the mouse paw and lung models, eupafolin effectively suppressed the LPS-induced edema formation and down-regulated iNOS and COX-2 expression. These results demonstrated that eupafolin exhibits anti-inflammatory properties and suggested that eupafolin can be developed as an anti-inflammatory agent.
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页数:15
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